Systemic cellular immunity and neuroinflammation during acute flare-up in multiple sclerosis and neuromyelitis optica spectrum disorder patients.

Twenty-seven treatment-naïve patients with relapsing-remitting multiple sclerosis (MS) and 13 with neuromyelitis optica spectrum disorder (NMOSD) were enrolled during a time of acute flare-up. Common cerebrospinal fluid (CSF) features were increased CD29- and/or CD45RO-positive helper T cells capable of propagating inflammation in the central nervous system (CNS). B cell activation in the CSF was unique to MS, while an increase in CD4CD192 (CCR2) cells in blood and breakdown of the blood-brain barrier (BBB) characterized NMOSD.

HLA genotype-clinical phenotype correlations in multiple sclerosis and neuromyelitis optica spectrum disorders based on Japan MS/NMOSD Biobank data.

HLA genotype-clinical phenotype correlations are not established for multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD). We studied HLA-DRB1/DPB1 genotype-phenotype correlations in 528 MS and 165 NMOSD cases using Japan MS/NMOSD Biobank materials. HLA-DRB1*04:05, DRB1*15:01 and DPB1*03:01 correlated with MS susceptibility and DRB1*01:01, DRB1*09:01, DRB1*13:02 and DPB1*04:01 were protective against MS.

Rheumatoid meningitis developed in patient with stable rheumatoid arthritis and myasthenia gravis-detailed analysis of intracranial inflammation using flow cytometry.

Background: Rheumatoid meningitis (RM) is a rare disorder that often develops during a remission phase of rheumatoid arthritis (RA). This is the first study to demonstrate differences in regard to immunological disturbance between blood and cerebrospinal fluid (CSF) samples obtained from a patient with RM using flow cytometry.

Case Presentation: A 36-year-old woman with RA and generalized myasthenia gravis (MG) developed RM during a remission phase.

[Anti-NMDA Receptor Antibody-Related Encephalitis].

Recently, the search for diagnostic antibody markers has drawn considerable attention in relation to autoimmune encephalitis. Among the antibody markers, the most frequently detected is the anti-N-methyl-D-aspartate receptor (NMDAR)antibody. Patients with this antibody develop characteristic clinical features.

Anti-neurofascin antibody in patients with combined central and peripheral demyelination.

Objectives: We aimed to identify the target antigens for combined central and peripheral demyelination (CCPD).

Methods: We screened target antigens by immunohistochemistry and immunoblotting using peripheral nerve tissues to identify target antigens recognized by serum antibodies from selected CCPD and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) cases. We then measured the level of antibody to the relevant antigen in 7 patients with CCPD, 16 patients with CIDP, 20 patients with multiple sclerosis, 20 patients with Guillain-Barré syndrome, 21 patients with other neuropathies, and 23 healthy controls (HC) by ELISA and cell-based assays using HEK293 cells.

[Diagnosis of multiple sclerosis].

The prevalence of multiple sclerosis (MS) in Japan has been increasing in recent years, and general physicians should be alert for early and correct diagnosis of this disorder. For this purpose, the 2010 revisions to the McDonald criteria are helpful, as they employed simplified parameters for magnetic resonance imaging (MRI) findings to confirm dissemination in space (DIS) as well as dissemination in time (DIT). However, physicians must also carefully consider medical history, combinations of neurological symptoms and signs, and findings obtained from cerebrospinal fluid samples and/or electrophysiological tests for individual diagnoses.

Novel FUS mutation in patients with sporadic amyotrophic lateral sclerosis and corticobasal degeneration.

We report a patient with sporadic amyotrophic lateral sclerosis (ALS) with a novel fusion in malignant liposarcoma (FUS) gene mutation whose neurological signs were conspicuous left-sided rigidity and apraxia. A novel heterozygous guanine (G)-to-thymine (T) transition at position 1392, c.1392G>T, leading to a methionine-to-isoleucine substitution (p.

Phenytoin at optimum doses ameliorates experimental autoimmune encephalomyelitis via modulation of immunoregulatory cells.

We investigated the optimum doses of phenytoin for treatment of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE). Oral and intraperitoneal administrations of 0.25 to 1.

[Case of anti P/Q type VGCC antibody positive small lung cell carcinoma that occured with subacute cerebellar degeneration, Lambert-Eaton myasthenic syndrome, and brainstem encephalitis].

A 62-year-old man was admitted to our hospital because of rapidly progressive dysarthria, truncal ataxia, and gait disturbance. High titers of the ProGRP and anti-P/Q-type VGCC antibody were detected in the serum. High accumulation of [18F] was detected at the hilus of the left lung on [18F]-FDG-PET scan.